Recent advances in molecular sequencing technology have allowed researchers to answer major questions regarding the relationship between a vast genomic diversity-such as found in the intestinal microflora-and host physiology. Over the past few years, it has been established that, in obesity, type 1 diabetes and Crohn's disease-to cite but a few-the intestinal microflora play a pathophysiological role and can induce, transfer or prevent the outcome of such conditions. A few of the molecular vectors responsible for this regulatory role have been determined. Some are related to control of the immune, vascular, endocrine and nervous systems located in the intestines. However, more important is the fact that the intestinal microflora-to-host relationship is bidirectional, with evidence of an impact of the host genome on the intestinal microbiome. This means that the ecology shared by the host and gut microflora should now be considered a new player that can be manipulated, using pharmacological and nutritional approaches, to control physiological functions and pathological outcomes. What now remains is to demonstrate the molecular connection between the intestinal microflora and metabolic diseases. We propose here that the proinflammatory lipopolysaccharides play a causal role in the onset of metabolic disorders.

Increasingly, studies are showing that changes in the microflora content of the digestive tract can be linked to metabolic illnesses, including type II (adult onset) diabetes and obesity. Blood group and secretor status play an important role in conditioning the overall characteristics of the digestive tract, including influencing the appearance and frequency of many strains of bacteria.

Pathol Biol (Paris). 2008 Jul;56(5):305-9. Epub 2008 Jan 30.
Role of gut microflora in the development of obesity and insulin resistance following high-fat diet feeding.

Cani PD, Delzenne NM, Amar J, Burcelin R.

A recent growing number of evidences shows that the increased prevalence of obesity and type 2 diabetes cannot be solely attributed to changes in the human genome, nutritional habits, or reduction of physical activity in our daily lives. Gut microflora may play an even more important role in maintaining human health. Recent data suggests that gut microbiota affects host nutritional metabolism with consequences on energy storage. Several mechanisms are proposed, linking events occurring in the colon and the regulation of energy metabolism. The present review discusses new findings that may explain how gut microbiota can be involved in the development of obesity and insulin resistance. Recently, studies have highlighted some key aspects of the mammalian host-gut microbial relationship. Gut microbiota could now be considered as a "microbial organ" localized within the host. Therefore, specific strategies aiming to regulate gut microbiota could be useful means to reduce the impact of high-fat feeding on the occurrence of metabolic diseases.

It has been known for quite a while that the colons of obese individuals are considerably longer than non-obese people. Now the idea is increasingly being advanced that obesity is, in part, related to greater "energy harvest." This would appear to throw the time-honored "just eat less and exercise more" argument right out the window and verify the common observance that many overweight people do not consume any greater amount of calories than many non-obese people.

Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.

Obesity is a worldwide epidemic, threatening both industrialized and developing countries, and is accompanied by a dramatic increase in obesity-related disorders, including type 2 diabetes mellitus, hypertension, cardiovascular diseases, and nonalcoholic fatty liver disease. Recent studies have shown that the gut microbial community (microbiota) is an environmental factor that regulates obesity by increasing energy harvest from the diet and by regulating peripheral metabolism. However, there are no data on how obesogenic microbiotas are established and whether this process is determined during infancy. The sterile fetus is born into a microbial world and is immediately colonized by numerous species originating from the surrounding ecosystems, especially the maternal vaginal and fecal microflora. This initial microbiota develops into a complex ecosystem in a predictable fashion determined by internal (eg, oxygen depletion) and external (eg, mode of birth, impact of environment, diet, hospitalization, application of antibiotics) factors. We discuss how the gut microbiota regulates obesity and how environmental factors that affect the establishment of the gut microbiota during infancy may contribute to obesity later in life.